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Category: genetics

Jumping DNA Sequences Drive Early Tumor Growth

New research reveals that LINE-1 retrotransposons don’t just nudge genes, they also trigger massive structural upheavals early in cancer development.

Read about the findings.

Where there’s a bountiful host, there are parasites ready to take advantage of the resources. This holds true even at microscopic levels. Lying within human DNA are repetitive elements called LINE-1 (L1) retrotransposons that promote their own propagation at the cost of the host organism’s health.1 These genetic parasites create copies of themselves that then get inserted at new locations within the genome. Until recently, scientists thought that the activity of L1s mostly resulted in local alterations to genes.

Now, in a new study published in Science, researchers have demonstrated that L1s can trigger dramatic structural changes in DNA, resulting in cancer-causing mutations.2 These findings, which shed light on the intricate relationship between cancer evolution and the genome, could lead to improved diagnostic and therapeutic strategies for different cancers.

“Cancer genomes are more influenced by these jumping fragments of DNA parasites than we previously thought,” said José Tubio, a molecular biologist at the University of Santiago de Compostela, in a statement.

Does suppression of HIV replication protect against severe M

tuberculosis infection?

Philana Ling Lin & team report on SIV/ART/TB models, finding antiretroviral treatment reduces pulmonary TB pathology, yet does not prevent extrapulmonary spread of TB.

1Department of Pediatrics, Children’s Hospital of Pittsburgh of the University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania, USA.

2Center for Vaccine Research.

3Department of Microbiology and Molecular Genetics, and.

4Division of Laboratory Animal Research, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA.

Continue reading “Does suppression of HIV replication protect against severe M” | >

Management of Inherited CNS Small Vessel Diseases: The CADASIL Example: A Scientific Statement From the American Heart Association

Lacunar infarcts and vascular dementia are important phenotypic characteristics of cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy, the most common inherited cerebral small vessel disease. Individuals with the disease show variability in the nature and onset of symptoms and rates of progression, which are only partially explained by differences in pathogenic mutations in the NOTCH3 gene. Recognizing the disease early in its course and securing a molecular diagnosis are important clinical goals, despite the lack of proven disease-modifying treatments.

Abstract: Emily Gutierrez-Morton

Yanchang Wang and colleagues (Florida State University) show that in yeast, polo-like kinase Cdc5 promotes the phosphorylation of SUMO protease Ulp2, reducing its affinity for SUMO chains and thereby facilitating polySUMOylation.

Genetics CellCycle

1Infectious Diseases Division, Department of Medicine and.

2Division of Plastic and Reconstructive Surgery, Washington University in St. Louis School of Medicine, St. Louis, Missouri, USA.

3Department of Mathematics, Dartmouth College, Hanover, New Hampshire, USA.

Immune cells selectively pull DNA from dying nuclei, revealing a process dubbed nucleocytosis

Over the years, cell biology has built a detailed picture of how cells compartmentalize their internal functions. Central to this organization is the nucleus, which houses the genetic material and is separated from the cytoplasm by a robust nuclear envelope.

Traditionally, the nuclear membrane has been considered a strict barrier, maintaining nuclear integrity except during carefully controlled processes such as mitosis. As a result, the release of nuclear material has largely been associated with cellular damage or death.

However, recent work by a research team in Japan suggests that this view may be incomplete.

‘Off the shelf’ immunotherapy could get a lift from gene-edited natural killer cells

Since scientists first discovered that human immune cells could be modified to become cancer-fighting agents, they’ve been trying to engineer a cell that’s effective against solid tumors, which account for the vast majority of cancer cases. In a key advance in meeting this “holy grail challenge” in the field of cancer cell therapy, a team of Yale scientists led by geneticist Sidi Chen has revealed how immune cells can be “boosted” to target and eradicate solid tumors.

The field of cell therapy began to revolutionize cancer treatment several decades ago, when researchers pioneered the use of therapeutic cells. In this process, immune cells are removed from a patient, modified so that they can better fight cancer, and then reintroduced into the patient’s body.

Two major streams of this therapy exist: CAR-NK cell therapy, which uses a patient’s natural killer (NK) cells, and CAR-T cell therapy, which uses a patient’s T cells. In both cases, scientists genetically modify the cells to express Chimeric Antigen Receptor (CAR), a synthetic receptor that helps immune cells recognize proteins on cancer cells.

The oncogenome of the domestic cat

Although cancer is a common cause of death in domestic cats, little is known about the range of cancer genes in cat tumors, and how this range might compare with the oncogenome in people.

Now, researchers in Science have sequenced cancer genes in 493 samples from 13 different types of feline cancer and matched healthy control tissue, gaining a clearer picture of the cat oncogenome and comparing the genes to known cancer-causing mutations in humans.

Cancer is a common cause of morbidity and mortality in domestic cats. Because the mutational landscape of domestic cat tumors remains uncharacterized, we performed targeted sequencing of 493 feline tumor–normal tissue pairs from 13 tumor types, focusing on the feline orthologs of ~1000 human cancer genes. TP53 was the most frequently mutated gene, and the most recurrent copy number alterations were loss of PTEN or FAS or gain of MYC. By identifying 31 driver genes, mutational signatures, viral sequences, and tumor-predisposing germline variants, our study provides insight into the domestic cat oncogenome. We demonstrate key similarities with the human oncogenome, confirming the cat as a valuable model for comparative studies, and identify potentially actionable mutations, aligning with a “One Medicine” approach.

FDA Greenlights Life Biosciences’ Human Study, Setting Up Pivotal Test for Aging Theory from Harvard’s David Sinclair

…Life Biosciences, a biotech company co-founded by Sinclair, received the FDA’s approval to begin a human trial testing its gene therapy based on the Information Theory of Aging. The gene therapy is designed to rewind the clock and restore the function of dying cells…

…Life Biosciences’ gene therapy has been under development for quite a while. In the 1990s, David Sinclair first contended that the deterioration and loss of epigenetic information—chemical tagging patterns on DNA that regulate which genes are turned on and off—plays an important role in driving aging. Sinclair subsequently dubbed this contention the Information Theory of Aging. Fast forward to the present day, and Life Biosciences has produced a gene therapy that delivers three proteins, which Sinclair’s laboratory helped establish, to reset epigenetic information to a more youthful state.

‘It’s extremely exciting,’ Sinclair told Endpoints News. ‘It’s been over 30 years to get to this point, and we’re about to learn if all of that work is going to come to fruition this year.’

The FDA has greenlighted Life Biosciences’ first human trial testing whether their gene therapy can confer a near-total rejuvenating reset of cells.

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